19.14B ). Hence, as pacing frequency is increased, the decrease in stroke volume must be approximately equal to the increase in heart rate. In addition, generalized vascular autoregulation tends to keep tissue blood flow constant (see also ). This adaptation leads to changes in preload and afterload that also keep cardiac output nearly constant.
Moreover, at excessively high pacing frequencies (above 200 beats/minute; see
Fig. 19.14 ), further increases in heart rate decrease cardiac output. Therefore, the induced decrease in stroke volume must have exceeded the increase in heart rate at this high range of pacing frequencies. At such high pacing frequencies, the ventricular filling time is so severely restricted that compensation is inadequate, and cardiac output decreases sharply. Although the relationship of cardiac output to heart rate is characteristically that of an inverted U in the general population, the relationship varies quantitatively among subjects and among physiological states.
Strong correlations between heart rate and cardiac output must be interpreted cautiously. In people who are exercising, for example, cardiac output and heart rate usually increase proportionately, and stroke volume may remain constant or increase only slightly (see the later section ”). It is tempting to conclude that the increase in cardiac output during exercise must be caused solely by the observed increase in heart rate. However,
Fig. 19.14 shows that over a wide range of heart rates, a change in heart rate may have little influence on cardiac output. The principal increase in cardiac output during exercise must therefore be attributed to other factors. Such ancillary factors include the pronounced reduction in peripheral vascular resistance because of the vasodilation in the active skeletal muscles and the increased contractility of cardiac muscle associated with the generalized increase in sympathetic neural activity. Nevertheless, the increase in heart rate is still an important factor. Abundant data show that if the heart rate cannot increase normally during exercise, the augmentation in cardiac output and the capacity for exercise are severely limited. Because stroke volume changes only slightly during exercise, the increase in heart rate may play an important permissive role in augmenting cardiac output during physical exercise.
Thecharacteristicrelationshipbetweencardiacoutputandheartrateexplainstheurgentneedoftreatmentbypatientswhohaveexcessivelysloworexcessivelyfastheartrates.Profoundbradycardia (slowrate)mayoccurasaresultofaveryslowsinusrhythminpatientswithsick sinus syndrome orasaresultofaslowidioventricularrhythminpatientswithcomplete atrioventricular block. Ineitherrhythmdisturbance,thecapacityoftheventriclestofillduringprolongeddiastoleislimited(oftenbythenoncompliantpericardium).Hence,cardiacoutputusuallydecreasessubstantiallybecausetheveryslowheartratecannotbecounterbalancedbyasufficientlylargestrokevolume.Asaconsequence,suchbradycardiaoftennecessitatestheimplantationofanartificialpacemaker.Inpatientswithsupraventricular orventricular tachycardia, excessivelyhighheartratesfrequentlynecessitateemergencytreatmentbecauseinsuchpatients,cardiacoutputmaybecriticallylow,andthefillingtimeissorestrictedatveryhighheartratesthatevensmalladditionalreductionsinfillingtimecausedisproportionatelyseverereductionsinfillingvolume.Slowingtheheartratetoamorenormalrhythmcangenerallybeaccomplishedpharmacologically,butelectricalcardioversionmayberequiredinemergencies(see
Ancillary Factors That Affect the Venous System﻿ and Cardiac Output